Neuro Flashcards
Multiple Sclerosis pathophys
progressive, autoimmune demylelination of central nerve fibers
onset of MS
20-40
risk factors for MS
female
1st degree relative
Epstein Barr Virus
other autoimmune disorders
smoking
triggers for MS
stress
elevated temps
postpartum period
s/s of MS
motor weakness, sensory disorders, visual impairment, autonomic instability
varies based on site of demyleination
treatment for MS
no cure
managed by corticosteroids, immune modulators, targeted antibodies
pre-anesthetic considerations for MS
assess existing deficits
if respiratory compromise - consider PFTs
Labs: CBC with platelets, BMP w/wo LFT
consider preop steroids
temperature management is crucial
avoid succinycholine
why might you draw a BMP with LFT on a MS patient
on dantrolene and azathioprine - causes bone marrow suppression, liver function impairment
*close attention to glucose and electrolyes as steroids may impact levels
what anesthetic plan might you have for a MS patient
General, regional, peripheral nerve block are acceptable options
what RSI agent would you avoid in MS
succinycholine - may induce HyperK+
upregulation of nACh receptors
what might hyperthemia do to an MS patient
preciptate an exacerbation of MS symptoms
Myasthenia Gravis Pathophysiology
autoimmune: antibodies generated against N-ACh-receptors at skeletal motor endplate
*no effect on smooth or cardiac muscle
which cranial nerves are commonly affected by myasthenia gravis? what effects do they have?
ocular (common) - diplopia, ptosis
bulbar - laryngeal/pharyngeal weakness leading to respiratory insuffiency, aspiration risk
when is maysthenia gravis (MG) muscle weakness exacerbated
w/ exercise
thymic hyperplasia in myasthenia gravis is common at _____% with _____% of patients improving with thymectomy
thymic hyperplasia in myasthenia gravis is common at 10% with 90% of patients improving with thymectomy
what can cause symptom exacerbation with myasthenia gravis
pain, insomnia, infection, surgery
stress
treatment of myasthenia gravis
ACh-E inhibitors (pyridostigmine), immunosuppressive agents, steroids, plasmapharesis, IVIG
MG preanesthetic considerations
assess existing deficits
if respiratory compromise, consider PFTs
optimize respiratory function
Labs: CBC, BMP +/- LFT
counsel pt on increased risk of postop vent support until fully recovered from anesthesia
4 medication considerations with MG
- reduce NMB dose to avoid prolonged muscle weakness
- caution with opioid to avoid respiratory compromise
- ACh-E inhibitors prolong succinycholine and ester LAs (X-caine)
- preop steroid with anyone on long term steroids
when would you add an LFT to MG chem panel
if the patient is on azathiporine
eaton-lambert syndrome pathophysiology
autoantibodies against VG Ca++Channels
-reduce Ca++ influx decreasing ACh release at the NMJ
> 60% of eaton lambert syndrome cases are associated with what
small cell lung carcinoma
s/s of Eaton Lambert Syndrome
progressive limb-girdle weakness, dysautonomia, oculbulbar palsy
treatment for eaton lambert syndrome
Selective K+ channel blocker
“3-4 diaminopyridine”
ACh-E inhibitors
Aziathioprine (immunologics)
Steroids
Plasmapheresis, IVIG
preanesthetic considerations for ELS (Eaton Lambert Syndrome)
assess exsisting deficits
if respiratory compromise - PFTs
optimize respiratory functoin
*extreme caution with NMB and opioid dosing
may need post-op respiratory support until fully recovered from anesthesia
consider regional
ELS and neuromuscular blockers
VERY SENSITIVE to ND-NMB and D-NMB
*significantly more sensitive to ND-NMB than MG patients
muscular dystophy pathophysiology
hereditary disorder of msucle fiber degerneration caused by breakdown of the dystophin-glycoprotein complex
- leading to myonecrosis, fibrosis, and skeletal membrane permeability
what is the most common and severe form of muscular dysrophy
who does it affect- onset & lifespan
Duchenne (DMD)
occurs only on boys, onset 2-5y
Wheelchair bound by 8-10 y
lifespan ~20-25 d/t cardiopulm complications
s/s of muscular dystrophy
progressive skeletal muscle wasting without motor/sensory abnormalities, kyphoscolosis, long bone fragility, respiratory weakness, frequent PNE, EKG changes
what lab is elevated in muscular dystrophy and why?
creatine kinase due to muscle wasting
what is myotonia
prolonged contractions after muscle stimulation, seen in several muscle disorders
most common myotonia
myotonic dystrophy
onset: 20-30 years
muscle wasting in face, masseter, hand, pre-tibial muscles & may effect pharyngeal, laryngeal, diaphragmatic muscles
cardiac conduction may be effected
what valvular disorder is seen in myotonic dystrophy
20% have mitral valve prolapse
myotnia congenita involves what muscles
involves skeletal (smooth/ cardiac muscles are spared)
(milder form)
what is central core disease
rare. core muscles cells lack mitochondrial enzymes
- proximal muscle weakness & scoliosis
what triggers myotonias
stress and cold temps
treatment for myotonias
no cure
managed with quinine, procainamide, steroids
preanesthetic condiserations for muscular dystrophies
CBC, BMP, PFTs, consider CK
preop EKG, ECHO - elvaluate for cardiomyopathy
drug condiserations for muscular dystrophies
caution with Non-depolarizing NMB (careful montiroing throughout)
hypermetabolic syndrome - similar to MH seen with sux and volatile anesthetics
can lead to rhabdo, HyperK+, vfib & cardiac arrest
Sux and VA may exacerbate instability of muscle membrane
consider lose dose Roc and TIVA for GA, Have MH cart with dantrolene available
pre anesthetic considerations for myotonic dystrophy (9)
- assess extent of CV and pulmonary abnormalities
- assess breath and heart sounds
- GI hypomotility (aspiration risk)
- high reaction of endocrine abnormalities (check thyroid and glucose levels)
- keep warm to avoid flares
- avoid Depolarizing NMB b/c fasiculations trigger myotonia
- caution with opioids
- optimize respiratory status
- incerased risk of postop respitatory weakness
3 major dementia syndromes
alzheimers (70%)
Vascular dementia (25%)
parkinsons (5%)
basic preop consierations with dementia patients
assess baseline level of cognitive dysfunction
- if patient unable to give informed consent look to medical POA
- investigate any advanced directives for medical decision making
- review basic labs and pertinent test/imaging
- potential aspiration risk (may be full stomach)
- increased risk for postop delirium (consider TIVA)
which preop meds need to be reviewed prior to anesthetic with dementia patients
ACh-I, MAOIs, psych meds
preferred anesthetic plan on dementia patietns
regional - decreased opioid requirement
balance opioids to meet analgesic requirement without exacerbating delirium
parkinson’s disease pathophysiology
degeneration of dopaminergic fibers of basal ganglia
unknown case. advanced age is the biggest risk factor
dopamine regulates the _________ by ____ _____ stimulation, which is stimulated by _______
dopamine regulates the extrapyramidal motor system by inhibiting exess stimulation, which is stimulated by ACh
T/F in parkinsons the motor neurons are under stimulated
false, in parkinon’s motor neurons are over stiumulated
triad of symptoms with parkinsons
skeletal muscle tremor, rigitidity, akinesia, posture
TRAP
other symptoms of parkinsons
pill roll tremor, facial rigidity, slurred speech, difficulty swallowing, respiratory difficutlty, depression, and dementia
treatment for parkinsons
Levadopa (cross BBB), anticholinergics, MAOIs (inhibit dopamine degredation), deep brain stimulator
preanesthetic considerations for parkinsons
assess severity with special attetention to respiratory compromise
review home meds (MAOIs)
basic labs along with PFT if respiratory symptoms
EKG, ECHO if indicated
increased aspiration risk (dysphagia, or possible dementia)
mediations to avoid in parkinsons patients
avoid reglan, phenothiazines, butyrophenones
avoid demerol if on MAOI
parkinsons home med to continue prior to surgery
PO levadopa must be continued to avoid unstable extrapyramidal effects such as chest wall rigidity
parkinsons patient with Deep brain stimulator considerations
- DBS may need to be disabled to avoid interaction with cautery
- if cautery used, biopolar recommended
in regards to brain tumors what can cause neurologic deficits
the mass effects!
increases ICP, papilledema, headache, mental impairment, mobility impairment, vomiting, autonomic dysfunction, seizures
brain tumors - pre anesthesia considerations
history, previous therapies, presenting symptoms & neurological deficits
radiation damage may lead to lethargy and AMS
chemoteraphy may also have neuro effects
CBC, BMP (glucose), EKG
CT/MRI
preop steroids and antiseizure per surgeon
why are patients w brain tumors on steroids
minimize cerebral edema
*continue steroids and monitor glucose
what diuretic is used to reduce ICP and pressure
mannitol
autonomic dysfunction from brain tumor may manifest on
EKG
labile HR and BP
anticonvulsants are common with which lesions
supratentorial lesions closer to motor cortex
cerebrovascular disease preop considerations
- review history, deficits, imaging, treatments, and co-existing disease
- assess orientation, pupils, bilateral grip stregnth, LE strength
- ask about headache, tinnitus, vision/memory loss, bathroom issues
- assess cause of CVA - vascular, embolic
- Imaging- carotid U/S, CT/MRI head and neck and ECHO
- preop EKG
- CBC, BMP (including glucose)
- cerebral oximetry
- Aline, 2 IV and/or CVC
what happens if the compensation for decreasing ICP fail
cerebral ischemia
subfalcine herniation
herniation of hemispheric contents under the flax cerebri
typically compressing branches of the anterior cerebral artery, creating a MLS
midline shift (MLS)
1
transtentorial herniation
herniation of the supratentorial contents past the tentorium cerebelli causing brainstem compression in a rostral to caudal direction
2
uncal herniation
subtype of transtentorial herniation
uncus (medial portion of temporal lobe) herniates over the tentorium cerebelli
4
herniation of cerebellar tonsils
occur due to elevated infratentorial pressure causing the cerebellar structure to herniate through the foramen magnunm
3
